Immune Network最新文献_第10页

Exosomal Communication Between the Tumor Microenvironment and Innate Immunity and Its Therapeutic Application. 肿瘤微环境与先天免疫的外泌体通讯及其治疗应用。

IF 6 4区医学

Immune Network Pub Date : 2022-09-26 eCollection Date: 2022-10-01 DOI: 10.4110/in.2022.22.e38

Hyunseok Kong, Sang Bum Kim

{"title":"Exosomal Communication Between the Tumor Microenvironment and Innate Immunity and Its Therapeutic Application.","authors":"Hyunseok Kong, Sang Bum Kim","doi":"10.4110/in.2022.22.e38","DOIUrl":"https://doi.org/10.4110/in.2022.22.e38","url":null,"abstract":"Exosomes, which are well-known nanoscale extracellular vesicles, are multifunctional biomaterials derived from endosomes and perform various functions. The exosome is a critical material in cell-cell communication. In addition, it regulates the pathophysiological conditions of the tumor microenvironment in particular. In the tumor microenvironment, exosomes play a controversial role in supporting or killing cancer by conveying biomaterials derived from parent cells. Innate immunity is a crucial component of the host defense mechanism, as it prevents foreign substances, such as viruses and other microbes and tumorigenesis from invading the body. Early in the tumorigenesis process, the innate immunity explicitly recognizes the tumor via Ags and educates the adaptive immunity to eliminate it. Recent studies have revealed that exosomes regulate immunity in the tumor microenvironment. Tumor-derived exosomes regulate immunity against tumor progression and metastasis. Furthermore, tumor-derived exosomes regulate polarization, differentiation, proliferation, and activation of innate immune cells. Exosomes produced from innate immune cells can inhibit or support tumor progression and metastasis via immune cell activation and direct cancer inhibition. In this study, we investigated current knowledge regarding the communication between tumor-derived exosomes and innate immune cell-derived exosomes (from macrophages, dendritic cells, NK cells, and neutrophils) in the tumor microenvironment. In addition, we discussed the potential development of exosomal immunotherapy using native or engineered exosomes against cancer.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":null,"pages":null},"PeriodicalIF":6.0,"publicationDate":"2022-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/26/0e/in-22-e38.PMC9634143.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40687729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Context-Dependent Regulation of Type17 Immunity by Microbiota at the Intestinal Barrier. 肠道屏障微生物群对 17 型免疫的情境依赖性调控

IF 4.3 4区医学

Immune Network Pub Date : 2022-09-26 eCollection Date: 2022-12-01 DOI: 10.4110/in.2022.22.e46

Begum Akuzum, June-Yong Lee

引用次数: 0

Engineering Cell Therapies for Autoimmune Diseases: From Preclinical to Clinical Proof of Concept. 治疗自身免疫性疾病的工程细胞疗法：从临床前到临床概念验证。

IF 4.3 4区医学

Immune Network Pub Date : 2022-09-21 eCollection Date: 2022-10-01 DOI: 10.4110/in.2022.22.e37

Sangwook Oh, Aimee S Payne

引用次数: 0

Outstanding Features of COVID-19 Overlapping Primary Immunodeficiency in Children. COVID-19重叠儿童原发性免疫缺陷的突出特征

IF 6 4区医学

Immune Network Pub Date : 2022-08-04 eCollection Date: 2022-08-01 DOI: 10.4110/in.2022.22.e30

Qi Jiang, Qian Yang, Man Man Niu, Peng Hu

引用次数: 1

Why Should We Consider Potential Roles of Oral Bacteria in the Pathogenesis of Sjögren Syndrome? 为什么我们应该考虑口腔细菌在Sjögren综合征发病机制中的潜在作用?

IF 6 4区医学

Immune Network Pub Date : 2022-08-03 eCollection Date: 2022-08-01 DOI: 10.4110/in.2022.22.e32

Sung-Ho Chang, Sung-Hwan Park, Mi-La Cho, Youngnim Choi

{"title":"Why Should We Consider Potential Roles of Oral Bacteria in the Pathogenesis of Sjögren Syndrome?","authors":"Sung-Ho Chang, Sung-Hwan Park, Mi-La Cho, Youngnim Choi","doi":"10.4110/in.2022.22.e32","DOIUrl":"https://doi.org/10.4110/in.2022.22.e32","url":null,"abstract":"Sjögren syndrome (SS) is a chronic autoimmune disorder that primarily targets the salivary and lacrimal glands. The pathology of these exocrine glands is characterized by periductal focal lymphocytic infiltrates, and both T cell-mediated tissue injury and autoantibodies that interfere with the secretion process underlie glandular hypofunction. In addition to these adaptive mechanisms, multiple innate immune pathways are dysregulated, particularly in the salivary gland epithelium. Our understanding of the pathogenetic mechanisms of SS has substantially improved during the past decade. In contrast to viral infection, bacterial infection has never been considered in the pathogenesis of SS. In this review, oral dysbiosis associated with SS and evidence for bacterial infection of the salivary glands in SS were reviewed. In addition, the potential contributions of bacterial infection to innate activation of ductal epithelial cells, plasmacytoid dendritic cells, and B cells and to the breach of tolerance via bystander activation of autoreactive T cells and molecular mimicry were discussed. The added roles of bacteria may extend our understanding of the pathogenetic mechanisms and therapeutic approaches for this autoimmune exocrinopathy.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":null,"pages":null},"PeriodicalIF":6.0,"publicationDate":"2022-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/d6/a1/in-22-e32.PMC9433196.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33454301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Omicron Subvariants, Including BA.4 and BA.5, Substantially Preserve T Cell Epitopes of Ancestral SARS-CoV-2. 包括BA.4和BA.5在内的组粒亚变体大量保留了祖先SARS-CoV-2的T细胞表位。

IF 6 4区医学

Immune Network Pub Date : 2022-08-03 eCollection Date: 2022-08-01 DOI: 10.4110/in.2022.22.e29

Kyemyung Park, Seung Jin Choi, Eui-Cheol Shin

{"title":"Omicron Subvariants, Including BA.4 and BA.5, Substantially Preserve T Cell Epitopes of Ancestral SARS-CoV-2.","authors":"Kyemyung Park, Seung Jin Choi, Eui-Cheol Shin","doi":"10.4110/in.2022.22.e29","DOIUrl":"https://doi.org/10.4110/in.2022.22.e29","url":null,"abstract":"https://immunenetwork.org The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron variants (B.1.1.529 and related) that emerged in November 2021 have spread worldwide, and are designated a variant of concern by the World Health Organization (WHO) (1). They have become the dominant strains, comprising >99% of newly deposited SARS-CoV-2 sequences in GISIAD (www. gisaid.org) as of May 16, 2022 (2). Following the emergence of B.1.1.529 (BA.1), BA.2 (often called stealth Omicron) soon became the most prevalent sublineage worldwide. Subsequent subvariants, including BA.2.9, BA.2.12.1, BA.4, and BA.5, are now rapidly dominating the circulating Omicron subvariants in originating regions, and are beginning to spread globally (2). The dominance of Omicron variants and their rapid evolution into various subvariants have raised concerns regarding the effects of the immunity elicited by natural infection or vaccination. As evolution continues, the variants’ spike proteins exhibit higher affinities toward ACE2, and/ or increasing capacity for evading preformed neutralizing antibodies induced by previous natural infection or vaccination (3-5). These changes are consistent with increased breakthrough infections and re-infections with Omicron variants (6,7).","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":null,"pages":null},"PeriodicalIF":6.0,"publicationDate":"2022-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/9a/2e/in-22-e29.PMC9433189.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33454304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 6

As a Modulator, Multitasking Roles of SIRT1 in Respiratory Diseases. SIRT1在呼吸系统疾病中的多任务调节作用

IF 6 4区医学

Immune Network Pub Date : 2022-06-20 eCollection Date: 2022-06-01 DOI: 10.4110/in.2022.22.e21

Yunxin Zhou, Fan Zhang, Junying Ding

{"title":"As a Modulator, Multitasking Roles of SIRT1 in Respiratory Diseases.","authors":"Yunxin Zhou, Fan Zhang, Junying Ding","doi":"10.4110/in.2022.22.e21","DOIUrl":"https://doi.org/10.4110/in.2022.22.e21","url":null,"abstract":"As far the current severe coronavirus disease 2019 (COVID-19), respiratory disease is still the biggest threat to human health. In addition, infectious respiratory diseases are particularly prominent. In addition to killing and clearing the infection pathogen directly, regulating the immune responses against the pathogens is also an important therapeutic modality. Sirtuins belong to NAD+-dependent class III histone deacetylases. Among 7 types of sirtuins, silent information regulator type-1 (SIRT1) played a multitasking role in modulating a wide range of physiological processes, including oxidative stress, inflammation, cell apoptosis, autophagy, antibacterial and antiviral functions. It showed a critical effect in regulating immune responses by deacetylation modification, especially through high-mobility group box 1 (HMGB1), a core molecule regulating the immune system. SIRT1 was associated with many respiratory diseases, including COVID-19 infection, bacterial pneumonia, tuberculosis, and so on. Here, we reviewed the latest research progress regarding the effects of SIRT1 on immune system in respiratory diseases. First, the structure and catalytic characteristics of SIRT1 were introduced. Next, the roles of SIRT1, and the mechanisms underlying the immune regulatory effect through HMGB1, as well as the specific activators/inhibitors of SIRT1, were elaborated. Finally, the multitasking roles of SIRT1 in several respiratory diseases were discussed separately. Taken together, this review implied that SIRT1 could serve as a promising specific therapeutic target for the treatment of respiratory diseases.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":null,"pages":null},"PeriodicalIF":6.0,"publicationDate":"2022-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/05/35/in-22-e21.PMC9250864.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40569100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4

Comparison of Waning Immunity Between Booster Vaccination and 2-Dose Vaccination With BNT162b2. 加强接种与2次接种BNT162b2免疫减弱的比较。

IF 6 4区医学

Immune Network Pub Date : 2022-06-17 eCollection Date: 2022-08-01 DOI: 10.4110/in.2022.22.e31

Jiwon Jung, Ji Yeun Kim, Ji-Soo Kwon, Sung-Cheol Yun, Sung-Han Kim

引用次数: 2

Tobacco Smoking Could Accentuate Epithelial-Mesenchymal Transition and Th2-Type Response in Patients With Chronic Rhinosinusitis With Nasal Polyps. 吸烟可增强慢性鼻窦炎合并鼻息肉患者的上皮-间质转化和th2型反应。

IF 6 4区医学

Immune Network Pub Date : 2022-06-15 eCollection Date: 2022-08-01 DOI: 10.4110/in.2022.22.e35

Ki-Il Lee, Younghwan Han, Jae-Sung Ryu, Seung Min In, Jong-Yeup Kim, Joong Su Park, Jong-Seok Kim, Juhye Kim, Jubin Youn, Seok-Rae Park

{"title":"Tobacco Smoking Could Accentuate Epithelial-Mesenchymal Transition and Th2-Type Response in Patients With Chronic Rhinosinusitis With Nasal Polyps.","authors":"Ki-Il Lee, Younghwan Han, Jae-Sung Ryu, Seung Min In, Jong-Yeup Kim, Joong Su Park, Jong-Seok Kim, Juhye Kim, Jubin Youn, Seok-Rae Park","doi":"10.4110/in.2022.22.e35","DOIUrl":"https://doi.org/10.4110/in.2022.22.e35","url":null,"abstract":"Tobacco smoking (TS) has been known as one of the most potent risk factors for airway inflammatory diseases. However, there has been a paucity of information regarding the immunologic alteration mediated by TS in patients with chronic rhinosinusitis with nasal polyps (CRSwNP). To identify the effect of TS, we harvested human tissue samples (never smoker: n=41, current smoker: n=22, quitter: n=23) and analyzed the expression of epithelial-derived cytokines (EDCs) such as IL-25, IL-33, and thymic stromal lymphopoietin. The expressions of Th2 cytokines and total serum IgE showed a type-2 inflammatory alteration by TS. In addition, the epithelial marker E-cadherin and epithelial-mesenchymal transition (EMT)-associated markers (N-cadherin, α-SMA, and vimentin) were evaluated. Histological analysis showed that EDC expressions were upregulated in the current smoker group and downregulated in the quitter group. These expression patterns were consistent with mRNA and protein expression levels. We also found that the local Th2 cytokine expression and IgE class switching, as well as serum IgE levels, were elevated in the current smoker group and showed normal levels in the quitter group. Furthermore, the expressions of E-cadherin decreased while those of N-cadherin, α-SMA, and vimentin increased in the current smoker group compared those in the never smoker group. Taken together, these results indicate that TS contributes to the deterioration of pathogenesis by releasing local EDCs and Th2 cytokines, resulting in EMT in patients with CRSwNP. We verified that alterations of immunological response by TS in sinonasal epithelium can play a vital role in leading to CRSwNP.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":null,"pages":null},"PeriodicalIF":6.0,"publicationDate":"2022-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/4f/8e/in-22-e35.PMC9433194.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33453823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

SOCS3 Attenuates Dexamethasone-Induced M2 Polarization by Down-Regulation of GILZ via ROS- and p38 MAPK-Dependent Pathways. SOCS3通过ROS-和p38 mapk依赖通路下调GILZ，减弱地塞米松诱导的M2极化。

IF 6 4区医学

Immune Network Pub Date : 2022-06-13 eCollection Date: 2022-08-01 DOI: 10.4110/in.2022.22.e33

Hana Jeong, Hyeyoung Yoon, Yerin Lee, Jun Tae Kim, Moses Yang, Gayoung Kim, Bom Jung, Seok Hee Park, Choong-Eun Lee

{"title":"SOCS3 Attenuates Dexamethasone-Induced M2 Polarization by Down-Regulation of GILZ via ROS- and p38 MAPK-Dependent Pathways.","authors":"Hana Jeong, Hyeyoung Yoon, Yerin Lee, Jun Tae Kim, Moses Yang, Gayoung Kim, Bom Jung, Seok Hee Park, Choong-Eun Lee","doi":"10.4110/in.2022.22.e33","DOIUrl":"https://doi.org/10.4110/in.2022.22.e33","url":null,"abstract":"Suppressors of cytokine signaling (SOCS) have emerged as potential regulators of macrophage function. We have investigated mechanisms of SOCS3 action on type 2 macrophage (M2) differentiation induced by glucocorticoid using human monocytic cell lines and mouse bone marrow-derived macrophages. Treatment of THP1 monocytic cells with dexamethasone (Dex) induced ROS generation and M2 polarization promoting IL-10 and TGF-β production, while suppressing IL-1β, TNF-α and IL-6 production. SOCS3 over-expression reduced, whereas SOCS3 ablation enhanced IL-10 and TGF-β induction with concomitant regulation of ROS. As a mediator of M2 differentiation, glucocorticoid-induced leucine zipper (GILZ) was down-regulated by SOCS3 and up-regulated by shSOCS3. The induction of GILZ and IL-10 by Dex was dependent on ROS and p38 MAPK activity. Importantly, GILZ ablation led to the inhibition of ROS generation and anti-inflammatory cytokine induction by Dex. Moreover, GILZ knock-down negated the up-regulation of IL-10 production induced by shSOCS3 transduction. Our data suggest that SOCS3 targets ROS- and p38-dependent GILZ expression to suppress Dex-induced M2 polarization.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":null,"pages":null},"PeriodicalIF":6.0,"publicationDate":"2022-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/d8/c3/in-22-e33.PMC9433193.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33454302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4